HIV is the etiological agent of what is commonly known as Acquired Immunodeficiency Syndrome (AIDS). HIV is an RNA retrovirus that has been given different names over the past several years, such as human T-lymphotropic virus III (HTLV-III); lymphadenopathy-associated virus (LAV); or AIDS-associated retrovirus (ARV). At the present time, HIV is being referred to as HIV-1 in order to differentiate it from a related virus designated HIV-2 (or LAV-2). For the purposes of this disclosure, the presently accepted designation HIV will be used to designate any viral agent that causes AIDS.
A characteristic of AIDS is the inability of the host immune system to effectively control virus replication, despite high levels of virus-specific antibodies, a subset of which are capable of neutralizing HIV in vitro. Nonetheless, patients possessing these antibodies and low levels of cytotoxic T cells appear to eventually succumb to the disease. Therefore, a better understanding of the HIV-1 antigenic determinants and their recognition by immune effector mechanisms would expedite the development of effective preventative and therapeutic modalities against AIDS.
Studies of experimental animal and human antibody responses to HIV have progressed quite rapidly, whereas the examination of T cell responses has lagged because of technical constraints, e.g., availability of highly active effector cells and appropriate infected targets. In order to identify regions within the HIV-1 envelope protein sequence that are capable of simulating immune effectors, in particular, T cells, applicants synthesized and examined a series of overlapping synthetic peptides derived from the carboxy-half of the gp120 envelope glycoprotein. Several such peptides have been identified which are capable of stimulating T cell proliferation.